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Bioenergetics of rat prostate cancer cell migration
Author(s) -
Kouvroukoglou Stylianos,
Lakkis Clair L.,
Wallace John D.,
Zygourakis Kyriacos,
Epner Daniel E.
Publication year - 1998
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19980201)34:2<137::aid-pros9>3.0.co;2-h
Subject(s) - bioenergetics , prostate cancer , prostate , medicine , cancer , biology , cancer research , endocrinology , pathology , microbiology and biotechnology , mitochondrion
BACKGROUND Increased cell motility and increased glycolysis are two well‐known hallmarks of cancer. We undertook these studies to determine whether increased glycolysis is required for prostate cancer cell locomotion. METHODS We studied the highly metastatic MatLu cell line, which is a variant of the Dunning R‐3327 rat prostate adenocarcinoma model. Using videomicroscopy and computer image analysis, we compared the speed of migration of cells grown in serum‐free medium in either the presence or absence of glucose. RESULTS We found that cells grown in glucose‐free, conditioned medium maintained speeds of migration and intracellular ATP levels for 24 hr which were equivalent to those of cells grown in conditioned medium containing glucose. In contrast, migration was significantly inhibited by growth in glucose‐free, un conditioned medium. We also tested the effect of antimycin A and rotenone, two inhibitors of mitochondrial electron transport, on cell migration and ATP levels. Antimycin A had no significant effect on either feature, while rotenone slightly inhibited cell migration without affecting ATP levels. CONCLUSIONS 1) Glycolysis is not necessary for rat prostate cancer cell locomotion in the presence of conditioned medium. 2) MatLu cells grown in the absence of both serum and conditioned medium require glucose to maintain cellular ATP levels and cell migration. 3) MatLu cells in conditioned medium adapt to inhibition of glycolysis or mitochondrial respiration by increasing the activity of the uninhibited pathway. Prostate 34:137–144, 1998. © 1998 Wiley‐Liss, Inc.